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-Hydroxylase Gene by Parathyroid Hormone, Calcitonin, and 1,25(OH)2D3 in Intact Animals1
The Institute of Molecular and Cellular Biosciences (A.M., K-i.T., S.K., Y.K., S.K.), The University of Tokyo, Yayoi 1–1-1, Bunkyo-ku, Tokyo 113-0032, Japan; Second Department of Internal Medicine (A.M., Y.K., T.H.), Jikei University School of Medicine, Nishishinbashi 3–25-8, Minato-ku, Tokyo 105-8461; CREST (S.K.), Japan Science and Technology Corporation, Honcho 4–1-8, Kawaguchi, Saitama 332-0012
Address all correspondence and requests for reprints to: Shigeaki Kato, Ph.D., The Institute of Molecular and Cellular Biosciences, The University of Tokyo, Yayoi 1–1-1, Bunkyo-ku, Tokyo 113-0032, Japan. E-mail: uskato{at}hongo.ecc.u-tokyo.ac.jp
Reflecting the prime role of 1
,25(OH)2D3 in
calcium homeostasis, the activity of 25-hydroxyvitamin D3
1-hydroxylase, a key enzyme for
1,25(OH)2D3 biosynthesis, is tightly
regulated by 1,25(OH)2D3, PTH and
calcitonin. Its significant activity is found in kidney, though the
enzymatic activity is also reported in extra-renal tissues. In the
present study, we found that the 1-hydroxylase gene abundantly
expresses in kidney, and at low levels in other tissues and in some
cell lines. Positive and negative regulations of 1-hydroxylase gene
by PTH, calcitonin, or 1,25(OH)2D3 were
observed at transcriptional levels in kidneys of animals and in a mouse
proximal tubule cell line. Moreover, the protein kinase A inhibitor
abrogated the PTH-mediated positive regulation. In mice lacking the
vitamin D receptor, the 1-hydroxylase gene expression was
overinduced, and the inducible effect of either PTH or calcitonin, but
not the repression by 1,25(OH)2D3, was
evident. Thus, vitamin D receptor is essential for the negative
regulation by 1,25(OH)2D3. Moreover, we
demonstrate that renal 1-hydroxylase gene expression in chronic
renal failure model rats was decreased and the positive effect by PTH
and calcitonin was diminished. The present study demonstrates that PTH
and calcitonin positively regulate renal 1-hydroxylase gene
expression via PKA-dependent and independent pathway, respectively, and
that 1,25(OH)2D3 negatively regulates it
mediated by vitamin D receptor. Furthermore, in a moderate state of
chronic renal failure, renal cells expressing the 1-hydroxylase gene
appear to have diminished potential in response to PTH and calcitonin.
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